Phys Exam 2 Flashcards
(348 cards)
1
Q
Nonmodifiable risk factors or CVD
A
Gender, age, family history
2
Q
Modifiable risk factors of CVD
A
Hypertension, dyslipidemia, cigarette cooking, obesity (metabolic syndrome, diabetes ,management), physical activity, sleep disorders, mental stress and depression, oral health.
3
Q
Materials transported in the cardiovascular system
A
Oxygen, nutrients and water, wastes, immune cells, antibodies, clotting proteins, hormones, stored nutrients, metabolic wastes, heat, CO2
4
Q
Closed loop system
A
Several “sub loops” or sections within the CV circulation have unique functional significance. Systemic system, coronary system, portal systems.
5
Q
What is a pulmonary embolism
A
A clot in the pulmonary system
6
Q
What is the difference between a traveling and stationary clot
A
An embolism is a solid fragment traveling through vessels until it gets lodged into a narrow vessel and becomes a clot.
7
Q
Clot on the venous side of circulation
A
Will always result in a pulmonary embolism
8
Q
Portal systems
A
Any part of the systemic circulation in which blood draining from the capillary bed of one structure flows through a larger vessel to supply the capillary bed of another structure before returning to the heart. Departing, renal, hypothalamic-hypophyseal.
9
Q
Does the venous or arterial system have a higher pressure
A
Arterial
10
Q
Average pressure in arteries is
A
Approximately 10th mmHg
11
Q
Average pressure in veins
A
0 mmHg
12
Q
What way does blood/fluid flow
A
Down a pressure gradient
13
Q
During the final months of pregnancy is its best for the mother to sleep in which position? Why?
A
Lying on the left side because it avoids compression of the vena cava
14
Q
What is static system pressure influenced by
A
Fluid volume, wall compliance
15
Q
What is a static system pressure influenced by
A
Fluid volume and wall compliance (stretch-ability)
16
Q
What is a flowing system pressure influenced by
A
Driving force/pressure, pressure gradient, resistance to flow.
17
Q
What influences resistance to flow
A
Diameter of vessel, total length of vessel, viscosity of fluid
18
Q
What affects wall compliance of vessels
A
Age, plaque B/U, some genetic factors.
19
Q
What is the driving force of blood pressure
A
Pressure created by heart muscle contractions in the ventricle moves the blood
20
Q
What chamber of the heart drives systemic circulation
A
Left ventricle
21
Q
**Flow is __________ proportional to the change pressure gradient and ________ proportional to the resistance of flow
A
Directly and inversely
22
Q
What results in increased flow
A
Higher system pressure gradient
23
Q
What decreases flow
A
Higher resistance
24
Q
Resistance to flow
A
Is a function of vessel length, blood viscosity, vessel diameter.
25
What is the most significant influence on resistance
Radius/diameter of the vessel
26
What happens to this pressure if the blood vessels constrict
Blood pressure increases
27
What happens to blood pressure if blood vessels dilate
Blood pressure decreases
28
What controls blood vessel radius/diameter
Autonomic nervous system? Sympathetic and parasympathetic
29
Additional changes to _________ and __________ can also affect blood pressure
Volume of blood and vessel wall compliance
30
What happens to blood pressure when someone is dehydrated or is taking a diuretic medication
Blood pressure decreases
31
Which organ system of the body is most responsible for regulation blood volume
Kidneys
32
How would atherosclerosis of numerous arteries affect blood pressure
Increases it
33
How much does small vessel change in radius change resistance to flow
To the 4th power
34
If the radius of tube A changes from 1 to 3 what happens
Resistance changes to 1/3^4
35
flow rate equals
The volume of blood that passes a given point in the system per unit time
36
Flow velocity
Is the distance a fixed volume of blood travels in a given period of time
37
at a constant flow rate ….
The velocity of flow through a small tube will be faster than through a larger tube
38
Major component of the heart
Myocardium
39
Atrioventricular valves
Between atria and ventricles. Tricuspid of right and bicuspid on left
40
Semilunar valves
Between ventricles and the two main arteries exiting the heart. Aortic and pulmonary
41
What is the function of the papillary muscles and Cordae tendinae
They connect to valves and hold them closed to prevent back flow
42
Myocardial contractile cellls
Majority of heart cells and are striated fibers organized into sarcomeres
43
Myocardial autorythmic cells (pacemaker cells)
Approximately 1% of heart cells. Smaller and fewer fibers and dont have sarcomeres. Signal contraction/set rate of beat.
44
SA node
Controls heart beat (70-80 BPM)
45
AV node
40-60 bpm, if the SA node is not working the AV node can take over and get enough blood to the brain
46
Bundle branches and purkinje fibers
20-40 bpm. These cells can contract on their own but not enough to keep the heart going
47
What neurons control the heart
Autonomic
48
What is the hormonal influence on contraction of the heart
Epinephrine
49
Contraction speed of the heart
Intermediate compared to skeletal and smooth
50
Does the force of myocardial contractile cells vary
Yes. Force generated by cardiac muscle is proportional to the number of myosin/actin cross bridges that are active.
51
What is the number of active cross bridges in cardiac muscle determined by
The amount of Ca++ available to bind to troponin
52
Where does intracellular Ca++ come from in cardiac muscle
The sarcoplasmic reticulum
53
How can you increase contraction of the heart
Increase stretch
54
Myocardial contractile cell similarities to neurons and skeletal muscle cells
Depolarization is die to Na+ entry and repolarization is due to K+ exiting.
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Myocardial contractile cell difference from neuron and skeletal muscle cells
Long AP (plateau) die to Ca++ entry in the cell to prevent tetanus.
56
What is tetanus and why is it important that the heart contraction does not reach a state of tetanus
A continuous tonic spasm of a muscle—it could result in fainting at minimum but could be fatal because the heart would be unable to pump blood to the brain.
57
Phases of myocardial contractile cell action potential
0-depolarization, Na+ channels open
1-initial repolarization, Na+ channels close
2-repolarization plateau, Ca++ channels open;fast K+ channels close
3-rapid repolarizatoin, Ca++ channels close; slow K+ channels open
4-RMP
58
How does lidocaine work in a local injection
Alters signal conduction in neurons by blocking the fast voltage gated Na channel in the neuronal cell membrane responsible for signal propagation
59
What is the greatest potential risk to performing too many intramural injections of lidocaine on a patient who is hypersensitive to the drug
Greatest risk is cardiac arrest, but more likely you will see decreased BP
60
What makes up the conducting system of the heart and what is the conducting system of the heart
Myocardial autorythmic cells and it is the SA, AV nodes and purkinje fibers
61
Pacemaker potential
Is an unstable membrane potential that cardiac autorythmic cells have.
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AP of cardiac autorythmic cells
Pacemaker potential phase: Na+ flows in through ion funny channels, hyperpolarization, as membrane potential slowly rises I F channels close and slow Ca++ open
Depolarization phase: threshold is reached AP occurs due to opening of fast gated Ca++ channels
Rapid repolarization:peak AP, Ca++ close and K+ channels open causing repolarization. K+ channels close at the end of this phase
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What effect would a drug that blocks the ion funny channels have on heart function
No response, heart rate would stop.
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How does the rising phase of an AP in the heart differ form smooth and skeletal muscle
The heart has Ca++ entry, the others have Na+
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What does ryania speciosa do
It enables calcium ions to exit the SR and enter the cytoplasm resulting in a sustained contracture of skeletal muscles w out depolarization of muscle cell membrane.
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How do depolarizations of autorythmic cells spread to adjacent contractile cells
Through gap junctions
67
What would happen to conduction if the AV node malfunctioned and could no longer depolarize?
The electrical signal from SA node would stop at the AV node, ventricle would not receive a signal. Purkinje fiber pacemaker would take over and produce a very slow beat
68
Electrical conduction of the heart
SA node—>internodal pathway from SA to AV—>AV node—>AV bundle—>bundle branches—>purkinje fibers
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How do the ventricles contract
From the bottom up
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Waves of an EKG
Reflect depolarization or repolarization of the atria and ventricles. P wave, Q wave, and T wave
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P wave
Atrial depolarization
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QRS complex
Progressive wave of ventricular depolarization (atrial repolarization)
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Q wave
Sometimes absent on normal EKG
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T wave
Ventricular repolarization
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Where is atrial repolarization represented on the EKG
It is part of the QRS complex but is overpowered by the ventricular activity
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Segments of an EKG
Sections of baseline between waves.
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Interval
A combination of a wave and segment
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P-R segment
Conduction through AV node and AV bundle
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What allows one to assess for abnormalities in an EKG
Segments
80
Are mechanical or electrical events lagging in the heart
Mechanical events lag slightly behind electrical
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What does the EKG represents
The summed electrical activity of all the heart muscle cells
82
Standard EKG speed
Runs 1mm per .04 seconds
83
Arrhythmia
Irregular interval lengths
84
How can you tell heart rate from an EKG
Time between two comparable waves on the tracing. P or QRS, just use a consistent one.
85
Normal serum potassium range
3.5-5.0 mmol/L
86
What are serum potassium levels outside the standard range associated with
Cardiac arrhythmias. Hypo and hyperkalemic states can put patients at risk for sudden cardiac death.
87
Hypokalemia on EKG
Significant hypokalemia is associated with Q-T interval prolongation and subsequent risk of ventricular fibrillation
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Hyperkalemia on EKG
Significant hyperkalemia is associated with peaked T waves and widened QRS complexes with subsequent risk for bradycardia and asystole.
89
What makes the “lub” sound
Closing of the AV valves
90
What makes dub sound
Closing of semilunar valves
91
Late diastole
Both sets of chambers relaxed and filling passively
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Atrial systole
Atrial contraction forces a small amount of blood (20%) into ventricles
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Isovolumetric ventricular contraction
First phase of ventricular contraction pushes AV valves closed but does not create enough pressure to open semilunar valves
94
Ventricular ejection
As ventricular pressure rises and exceeds pressure in the atria, the semilunar valves open and blood is ejected.
95
Isovolumetric ventricular relaxation
As ventricles relax, pressure in ventricles falls, blood flows back into cusps of semilunar valves and snaps them clsoed.
96
Diastole
Cardiac muscle relaxes
97
Systole
Cardiac muscle contracts
98
Where does the right atria receive blood from
SVC and IVC
99
Where does the left atria receive blood from
Pulmonary veins
100
During atrial systole what creates a visible pulse
Some blood being forced back into the vena cava in the jugular vein if someone is laying supine.
101
If someone is upright and you can see a pulse in the jugular vein what may be wrong
Above normal atrial pressure
102
Auscultation is using a stethoscope to listen to hear sounds through the chest wall. At which point in the heart cycle would you first begin to hear blood regurgitating through a faulty aortic SL valve back into the left ventricle
Isovolumetric ventricular relaxation
103
Does the L ventricle eject all of its blood by the end of ventricular systole?
No, there is always some blood in there. Around 65 mm
104
Stroke volume
Is the amount of blood pumped per contraction/beat
105
End diastolic volume
Is maximum amount of blood in a ventricle during a mechanical heart cycle
106
End systolic volume
Is the least volume of blood in a ventricle during a mechanical heart cycle
107
Why is there some residual blood left in the ventricle after systole?
Allows for compensatory change with change in vessel capacities. Safety mechanism.
108
How to find stoke volume
EDV-ESV
109
Is stroke volume a constant
No, it can increase up to 100mL during exercise and is controlled by many different factors
110
Cardiac output
Volume of blood pumped by one ventricle in a given period of time. BPM X SV
111
Four determinants of cardiac output
Heart rate
preload-more venous blood in
contractility-muscle contraction force
afterload-less vascular resistance out
112
What happens when one side of the heart begins to fail
Blood pools in the circulation behind the failing side because loss of cardiac muscle function
113
Heart rate
Highly variable, initiated by SA node, modulated by neuronal and hormonal input, SA node control typically dominated in the PNS.
114
What affect do sympathetic neurons have on HR
They bind to beta 1 receptors and increases Na+ and Ca++ influx, increase rate of depolarization, increase HR
115
What affect do parasympathetic neurons have on HR
Bind to muscarinic receptors and increase K+ efflex and decrease, decrease hyperpolarization cell and rate of depolarization, decrease HR
116
What does epinephrine do to hear rate
Depolarize the autorythmic cell and speed up the pacemaker potential, increasing the heart rate
117
How does an epi pen work
It relaxes smooth muscle in the airways to reduce wheezing and improve breathing. Constricts blood vessels which decreases swelling and increases BP
118
How do cholinergic agonist drugs or “parasympathetic drugs” work
Slows heart rate, causes vasodilation, constriction of pupils, secretion of sweat, saliva, tears, and mucus (in the respiratory tract) and constriction of bronchioles.
119
What part of the NS dominates tonic control of HR
Parasympathetic branch of the ANS
120
Chrontoropic
Means rate or timing of a physiological process. These drugs influence heart rate.
121
Chronotropic incompetence
Broadly defined as the inability of the heart to increase its rate commensurate with increased activity or demand
122
What controls the HR response during exercise
Catecholamines from the eternal glands, resulting in significantly slower increase of the HR at onset of exercise, reduced peak HR, and delayed return towards resting values after cessation of exercise.
123
What happens to nervous system control of heart rare in transplant patients especially during exercise
They faint because HR can’t adapt. Higher HR due to loss of parasympathetic control. Re-educated HR during exercise form chrontoropic incompetence due to denervation
124
Heart rate is under ANS and hormone control, this is also known as
Chronotropic
125
Preload and contractility are known are _______
Ionotropic
126
What determines preload
The volume of blood in the ventricular wall. Length tension relationship of myocardial cells.
127
What influences contractility of the heart
Influenced by stretch of muscle cells and chemical/electrical factors (drugs, hormones, SNS)
128
Frank starling law
States that stroke volume increases as EDV increase increases. EDV is determined by venous return. More ventricle stretch means more powerful contraction.
129
Venous return (preload) is affected by
Skeletal muscle pump, respiratory pump, sympathetic innervation of veins.
130
Skeletal muscle pump
Skeletal muscle contraction promotes venous return, especially in the lower limbs.
131
Respiratory pump
Lower atmospheric pressure in thorax with inhalation, decreases thoracic vena cava pressure which helps draw more blood into the vena cava. Also enhanced by higher abdominal pressure with diaphragmatic contraction.
132
Sympathetic innervation of veins
Vasoconstriction squeezes blood out of veins sending more blood into the right atrium of the heart
133
Length-tension relationships preload skeletal muscle
As skeletal muscle is stretched from very short lengths, its tension increases because excessive overlap of myofilaments is removed.
134
Length-tension preload relationship of cardiac muscle
As cardiac is stretched form very short lengths, its tension increases from removing interfering myofilament overlap and from increasing the number of active cross bridges by increasing sensitivity of myofilaments to Ca++
135
What is the difference in heart muscle tension development when it is stretched to 80% of maximum length compared to stretched at 95% max length
Cardiac muscle tension development/contractile force production is INCREASED significantly at 95% stretch compared to skeletal muscle. Necessary to pump additional fluid volumes
136
What is the length-tension relationship of preload known as
Starling curve
137
How would venous dilation affect stroke volume
Decreases stroke volume and reduces venous return
138
Inotropic
Modifying the force or speed of contraction of muscles. Any chemical that affects contractility is an inotropic agent
139
Positive inotropic drugs
Increase/strengthen contractility. Which pumps more blood with fewer heart beats.
140
What are positive inotropic drugs used for
For patients with congestive heart failure or cardiomyopathy. Sometimes given to patients who have had a recent heart attack to compensate for lost contractility due to heart muscle damage
141
Examples of positive inotropic drugs
Epinephrine, norepinephrine, and digitalis.
142
Local anesthetics are also commonly paired with epinephrine, why?
Due to vasoconstrictive effects. Helps prevent systemic spread of the anesthetic, increases the duration of anesthetic action, and may reduce local hemorrhaging from procedures performed.
143
Negative inotropic drugs
Decrease/weaken contractility, which means less blood pumped and slows heart rate.
144
Examples of negative inotropic drugs
Used for hypertension, chronic heart failure, arrhythmias, and angina. Beta blocker, calcium channel blockers, and antiarrhythmic medicines.
145
Catecholamines
Are hormones produced by the adrenal glands, they include epinephrine, norepinephrine, and small amounts of dopamine.
146
What happens to contractions with positive inotropic compounds
More forceful contraction that are shorter in duration.
147
After load
After load is the combined load of EDV and arterial resistance during ventricular contraction
148
Factors that affect afterlaod
Arterial constriction, loss of arterial wall compliance which can be caused by atherosclerosis.
149
What is an indirect measure of afterload
Blood pressure
150
Ejection fraction
Is the percentage of EDV ejected with one contraction
151
What is the typical ejection fraction for an average resting individual? What the normal range considered to be
About 55%, 55-70%
152
How to find Ejection fraction
Amount of blood pumped out of the ventricle/total amount of blood in ventricle=EF
153
What factor of cardiac output is most influenced by ACh
Heart rate and it decreases it
154
Which factor of cardiac output is most affected by norepinephrine/epinephrine
Heart rate and contractility and it causes them to increase
155
What cells have muscarinic receptors
Parasympathetic cells so the SA node autorythmic cells
156
How is the rate of blood flow to tissues controlled
In relation to the need of the tissue
157
Which circulatory system has a lower pressure
Pulmonary. Pulmonary resistance is about 10x less than systemic
158
How are new blood vessels created
Angiogenesis. Capillaries grow and regression healthy tissues according to functional demands
159
Windkessel effect
Sympathetic effect in large arteries and it is elastic vessels store potential energy when stretched during systole. During diastole, the elastic recoil of these vessels maintain as the forward flow of blood and organ perfusion between systoles.
160
What blood vessels have the greatest influence on total peripheral resistance and systemic BP through vasoconstriction/dilation
Arterioles
161
How is blood flow to capillaries regulated
Capillaries are not innervated by the SNS and blood flow to them is regulated by arterioles and pre-capillary sphincters
162
What vessels carry the largest volumes of blood
Veins
163
Do veins or arteries tend to have larger diameters
Veins
164
What are the most common diseases of mankind and what are they a key risk in
Oral infections and they are a key risk for heart disease
165
What governs the passive exchange of water between the capillary and micro circulation and the interstitial fluid
Starling forces
166
What determines the directionality of net water movement between two compartments and determines the rate at which water exchange occurs
Starling forces
167
A combination of relative hydrostatic pressure and on optic pressure determine what
Directions of water exchange between the plasma and interstitial fluid across the capillary wall. The rate of exchange is is governed by the permeability of the capillary wall itself
168
Hydrostatic pressure
Refers to the physical force of fluids against their enclosing barriers. Plasma within capillaries has a positive hydrostatic pressure. Fluid within the interstitial space generally has a negative hydrostatic pressure
169
Oncotic pressure gradient
Refers to the osmotic pressure generated by the presence of proteinacious solutes.
170
What is the affect of plasma proteins being unable to cross the capillary barrier
These osmotically active solutes are at a higher concentration I the plasma than in the interstitial fluid. Consequently the oncotic pressure within the plasma Is higher than in the interstitial fluid. This creates an oncotic pressure gradient between the two compartments.
171
Vascular permeability
The histological architecture of capillaries determine the permeability of capillaries to water and this can vary by over two orders of magnitude in different capillary beds.
172
For most capillary beds what happens to the starling forces as flood moves through the bed
They reverse
173
Starling forces cause _____ near the arteriolar side of the microcirculation
Outward fluid filtration
174
Starling forces cause __________ on the venous side of microcirculation
Fluid resorption
175
Capillary hydrostatic pressure
Is at its highest value nearest the high pressure arteries
176
Interstitial hydrostatic pressure
Is at its constant negative value
177
Net filtration of fluid on the arteriole side
Outward direction due to the outward hydrostatic pressure gradient is larger than the inward oncotic pressure gradient
178
Capillary hydrostatic pressure on the venous side _________ due to ______________ to blood flow generated by the capillary
Declines, resistance
179
Net filtration
Outward fluid filtration on the arterial side of the microcirculation largely balances inward fluid filtration on the venous side
180
How does localized and generalized edema occur
Excessive water filtration out of the capillaries locally adn generalized when it occurs globally throughout the body’s microcirculation
181
Derangements of vascular permeability
Occurs when the tight architecture of the capillaries is damaged. This can occur to do immune-mediated processes in acute inflammation of thermal damage in burns
182
Derangements of hydrostatic pressure gradient
Usually occur due to pathologically increased hydrostatic pressure on the venous side of the microcirculation due to ineffective venous draining of blood (back up of blood). Failing pump.
183
Derangements of oncotic pressure
Usually occurs die to reductions in plas,a oncotic pressure form poor synthesis of excessive loss of plasma proteins, especially albumin. Reduced OP reduces the inward oncotic gradient and allows for increased outward fluid filtration
184
How is systemic blood pressure created
By ventricular contraction, elastic recoil in arteries sustaining driving force, and blood flow obeying rules of fluid flow.
185
Blood flow is directly proportional to what and inversely proportional to what
The pressure gradient between any two points. Inversely proportional to the resistance in vessels.
186
Primary determinant of velocity in cardiovascular system
When flow rate is constant it is the total cross sectional area of the vessel
187
What are three factors affecting resistance
Radius of BV’s, viscosity of blood, and length of the system
188
Is diastole or systole longer
Diastole is twice as long as systole
189
Mean arterial pressure
Is an indirect measure of ventricular pressure
190
How is the flow of blood in veins influenced
One way valves ensure flow direction, skeletal muscle and diaphragm/respiratory muscles, gravity
191
Which of the following is most likely to cause your patient to experience orthostatic hypotension when getting up and out of a reclined chair
Dehydration. It causes low volume so overall pressure decreases
192
MAP is proportional to ___________ and _____________ in the arterioles
Cardiac output and peripheral resistance in the arterioles
193
Factors influencing mean arterial blood pressure
Blood flow into and out of the arteries (resistance to blood flow), distribution of blood between arteries and veins. Total blood volume, heart pump effectiveness
194
Veins as a volume reservoir
They can redistribute blood to arteries if needed. increased SNS activity can constrict veins which increases blood volume returned to heart. This increases EDV and cause heart to increase SV
195
Arteriolar resistance is directly proportional to what and inversely proportional to
Length of vessel, viscosity of blood and inversely proportional to vessel radius.
196
What percentage of resistance to blood flow do arterioles account for
60%
197
Local control of arteriolar resistance
Regulate local blood flow to the capillaries in response to the local tissues metabolic needs via cell signaling known as “paracrine” signals.
198
Systemic control of arteriolar resistance
ANS sympathetic relfexes—CNS mediated, MAP maintenance and body temp homeostasis. Controlled by hormones—-particularly salt/electrolyte and water homeostasis
199
Norepinephrine
Baroreceptor refelx, sympathetic neurons, neurotransmitter
200
Epinephrine
Increase blood flow to skeletal muscle, heart, and liver. Adrenal medulla produces it. It’s a neurohormone.
201
Nitric oxide
Paracrine mediator. Endothelium produces it. Paracrine
202
Histamine
Increases blood flow. Produced by mast cells. Is paracrine.
203
Myogenic autoregulation
Intrinsic ability of a vessel to control its state of contraction to help maintain a constant blood flow to capillaries.
204
If blood pressure increases in an arteriole….
The resultant stretch of the vessel wall signals the smooth muscle to constrict and decrease blood flow through the vessel.
205
If blood pressure decreases in an arteriole….
Blood flow initially falls. When blood flow falls, the vessels will dilate to increase blood flow to the local area.
206
Adenosine
Released by cardiomyocytes low on O2
207
Histamine
Vasodilator as part of inflammatory response
208
Seratonin
Vasoconstrictor released by platelets
209
What is the most commonly observable sign of any type of hyperemia
Redness
210
Active hyperemia
Increased blood flow associated with increased metabolic tissue activity I.e, exercise.
211
Reactive hyperemia
Decrease in tissue blood from due to occlusion. Arterioles dilate but occlusion prevents blood flow.
212
The greatest percentage of blood flows through which body organ
Liver and digestive tract
213
If you have four vessels and B constricts what happens to the pressure proximally and distally
Proximally the pressure increases and distally it decreases. Flow will also be diverted from constricted vessel B and divided among other vessels
214
What Is a baroreceptor reflex sensitive to
Pressure changes
215
Baroreceptor reflex response to increased BP
Firing of Baroreceptor in carotid arteries and aorta, sensory neurons receive signal, cardiovascular control center in medulla oblongata increase parasympathetic control and produce more ACh on muscarinic receptors to decrease force of contraction, heart rate, CO, and overall BP. Decreased sympathetic activity causes less NE to be released causing vasodilation and decreased peripheral resistance and decreasing BP
216
SNS neurotransmitters and receptors involved in teh baroreceptor reflex
Norepinephrine and alpha receptors on arterioles and veins and beta receptors on ventricular myocardial can SA nodal cells
217
PNS neurotransmitter and receptor
Acetylcholine and and muscarinic receptors on SA node
218
What is syncope
Fainting
219
What is the basic cause of syncope
No blood to brain
220
Vasovagal syncope
CV system overreaction to certain emotional triggers such as fright or emotional distress. It’s also called neurocardiogenic syncope
221
Causes of syncope
Dehydration, SNS system dysfunction, ANS atrophy, CNS related dysfunction affecting hypothalamus (Parkinson’s or tumor), extreme emotional response, heart failure.
222
Immediately following the injection, J.K. begins sweating and he reports that his heart is racing and he feels nervous. You must act quickly!
1. What do you think has happened to your patient? What is he most likely experiencing:
After sitting J.K. up from the supine position, he reports a crushing pain in his chest and a numb sensation extending down his left arm. What should you do?
What is the most likely cause of J.K.’s pain?
Why does tachycardia decreases the perfusion of the coronary circulation because
1-the fight or flight response due to injection
2-immediately call 911
3-an increase in heart rate
4-the amount of time the ventricles spend in diastole is decreased over the span of a minute
223
Functions of the respiratory system
Exchange of gasses between atmosphere and blood, homeodynamic regulation of body temp and pH, protection from inhaled pathogens and irritating substances, helps with vocalization.
224
How is the respiratory system not Ike the CV system
There is no muscular pump, and it uses muscles to created pressure gradients
225
What muscles in the respiratory system are used to create pressure gradients
Mainly the diaphragm
226
Poiseuille’s law for fluid
It’s also applicable to airflow. It states that the flow of a fluid is related to the viscosity, the pressure gradient across the tubing and the length and diameter of the tubing.
227
External respiration
Is the movement of gases between the environment and body’s cell
228
Cellular respiration
Is the intracellular reaction of oxygen with organic molecules to produce CO2, water, and ATP.
229
Conducting zone
Provides rigid conduits for air to reach the sites of gaseous exchange. Includes nose, pharynx, larynx, trachea, bronchi, bronchioles and terminal bronchioles. No gas exchange is conducting zone, just warming and humidifying of air.
230
Respiratory zone
Site of gaseous exchange. Structures include respiratory bronchioles, alveolar duct, and alveoli.
231
How does persistent mouth breathing influence your patients dentition
Dries out the oral cavity resulting in reduced protection from acidity
232
What are some benefits of nasal breathing
Nasal passage designed to warm and humidify. Helps removes a significant share of germs, bacteria adn irritants. Keeps air in your lungs a little longer because of resistance when exhaling and allows for more O2 to enter bloodstream. nitric oxide plays an import role in immune response and case regulation is released into the nasal passages.
233
When are muscles of expiration needed
Only during forced breathing
234
Muscles of quiet inspiration
Diaphragm
235
Muscles of inspiration during exercise
Diaphragm, external intercostal, scalene, sternocleidomastoid
236
Muscles of expiration during exercise
Abdominal muscles, internal intercostals
237
What does the activity of accessory inspiration muscles in a person indicate
Something wrong w/pulmonary system—>emphysema
238
Which muscles are strengthened by blowing up balloons
External and internal obliques and abdominus rectus
239
Functional unit of the respiratory system
Alveoli
240
Blood air barrier
Exists in the gas exchange region of the lungs and the fused basement membranes of the type 1 pneumocytes and endothelium prevent air bubbles form forming in the blood and from blood entering alveoli.
241
What is the trachea lined with
Pseudostratified ciliated columnar epithelium and goblet cells interspersed
242
Function of the cilia in the airway
Move mucous towards pharynx, removing trapped pathogens and particulate matter.
243
Secretions of the airway
Mucous by goblet cells, seromucous cells and epithelial cells secrete saline.
244
Key ion channels in saline secretion by airway epithelial cells
NKCC ( Na+, K+, 2Cl-)and CFTR
245
Saline secretion by airway epithelial cells (process)
1- NKCC brings Cl- into epithelial cell from ECF
2-apical anion channels including CFTR allow Cl-to enter lumen
3-Na+ goes from ECF to lumen by paracellular pathway,drawn by the electrochemical gradient
4-NaCl movement form ECF to lumen creates a concentration gradient so water follows into the lumen
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Oral implications associated with cystic fibrosis
Enamel hypoplasia and tooth discoloration, salivary gland involvement, reservoir for potentially pathogenic respiratory bacteria.
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Dalton’s law
States that the total pressure of a mixture of gases is the sum of the pressures of individual gases (partial pressures).
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Effect of water vapor on partial pressures
Decreases and dilutes partial pressures
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Boyles law
States that the pressure of a gas tends to increase as the volume of the container decreases.
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Application of boyles law to lungs
To decrease pressure inside a chest cavity the lungs expand and increase their volume which creates a pressure gradient. The process reverses when lungs contract
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During fetal development what happens to the thoracic cage and parietal pleura
They grow more rapidly than the lung with its visceral pleura leading a negative pleural cavity pressure
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What maintains the subatmospheric intrapleural pressure
Two opposing forces, elastic recoil of the lung creating an inward pressure and the chest wall pulling outward
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Pleural membrane
Functionally connects lungs to the chest wall so that chest wall expansion expands the lungs
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Pleural fluid
Serves as a lubricant so lungs can move freely in the chest wall
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Breathing mechanics of inspiration
Contraction of; diaphragm, external intercostal and scalene muscles. Leads to an increase in thoracic volume, decrease in air pressure, and then air moves into the lungs
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Breathing mechanics expiration
Inspiration muscles relax leading to a decrease in thoracic volume, increase in pressure and outward movement of air. Expiration is a passive phenomenon when resting.
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Alveolar pressure
Pressure in your alveoli
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Intrapleural pressure
Pressure between pleural membranes
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Normally, expiration takes _______________ than inspiration
2-3 X longer.
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Residual volume
Leftover air after a complete exhale
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Expiratory reserve volume
Amount of air you can expel after a normal expiration
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Tidal volume
Normal breathing
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Inspiration reserve volume
Volume you can breath in after normal inspiration
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How do you measure vital capacity
With a spirometer
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Pneumothorax
A collapsed lung that cannot function normally
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Total lung capacity
tidal volume+IRV+ERV+RV
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What happens if air or fluid enters the space between parietal and visceral linings
The lung can collapse because the pressure in the pleural space will no longer be negative to the external atmospheric pressure
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What two ways can you get a pneumothorax
Penetrating wound of rib fracture or leaking of air form the lung itself.
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Compliance
Ability to stretch
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Elastance
Ability to recoil
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Restrictive lung diseases
Lungs unable to fully expand/inhale; fibrotic lung disease, scoliosis or severe obesity, inadequate surfactant production
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Obstructive lung diseases
Unable to exhale normally; emphysema/COPD, asthma
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How does emphysema affect compliance and elastance
Increases compliance and decreases elastance
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How does fibrosis affect compliance and elastance
It decreases compliance and has no affect on elastance
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Forced expiratory volume in one second (FEV1)
Shows the amount of air a person can forcefully exhale in one second of the FVC test. This can help diagnose disease severity
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A premature infant lack surfactant, how would this affect inspiration reserve
Decrease IRV
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How would moderate emphysema affect an individuals residual lung volume
It would increase it because they are unable to move air out
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Obstructive lung disease treatment
Purse-lip breathing can help control oxygenation and ventilation. Inspire through the nose and exhale through the mouth with pursed lips at a slow controlled rate. It keeps small airways open during exhalation
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What reduces surface tension in the lungs
Surfactant
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Surface tension
Greater attraction of liquid molecules to each other than to the molecules in the air.
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Law of LaPlace
The pressure inside an inflated elastic container with a curved surface is inversely proportional to the radius if the surface tension remains constant
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What would happen if alveoli had the same amount of surfactant
The alveoli with the smaller radius would have higher pressure and vice versa leading to air flow form smaller alveoli to larger
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What alveoli produce more surfactant
Smaller alveoli
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What cells secrete surfactant and what is it made of
Type II alveolar cells. A mixture containing proteins and phospholipids and it disrupts cohesive forces between water molecules.
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Newborn respiratory distress syndrome
Inadequate surfactant concentrations in premature babies
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Parameters contributing to resistance in respiratory system
Resistance, length, viscosity of the substance flowing, radius.
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What affects the diameter of the upper airway
Physical obstruction
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What affects the diameter of the bronchioles
Bronchodilation-CO2, epinephrine, beta receptors
bronchoconstriction-parasympathetic neurons, histamine, leuoktrines, muscarinic receptors
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Alveolar dead space
Areas of conducting zone that do not exchange gas with blood are known as atomic dead space
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Pulmonary ventilation
Ventilation rate X tidal volume
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Alveolar ventilation
Ventilation rate X (tidal volume- dead space volume)
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Eupnea
Normal quiet breathing
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Hyperpnea
Increased respiratory rate and or volume in response to increased metabolism (exercise)
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Hyperventilation
Increased respiratory rate and/or volume without increased metabolism
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Hypoventilation
Decreased alveolar ventilation
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Tachypnea
Rapid breathing usually increased respiratory rates with decreased depth
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Dyspnea
Difficulty breathing (a subjective feeling sometimes described as “air hunger”
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Apnea
Cessation of breathing—issue with pulmonary control center in medulla
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What happens to blood if it flows past an under ventilated alveoli
It does not get oxygenated, leading to a constriction of arterioles so that the blood is diverted to a better ventilated alveoli
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Changes in bronchiole diameter is mediated primarily by what
Levels of CO2 in the exhaled air passing through them.
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In the arterial blood, pO2 is ____________ than that of the _______ so O2 moves _________
Lower than that of the alveoli so O2 moves down its concentration gradient
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Tissue pO2 is ..
Lower than that of the blood so O2 moves down its concentration gradient
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Isn’t the venous blood pCO2 is…
Higher than that of the alveoli so CO2 moves down its concentration gradient which is exhaled out
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Hypoxia hypoxia
Low arterial pO2. High altitude or alveolar hypoventilation, decreases lung diffusion capacity can cause this
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Anemic hypoxia
Decreased total amount of O2 bound to hemoglobin. Caused by blood loss, anemia, or altered hemoglobin binding.
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Ischemic hypoxia
Reduced blood flow. Can be caused by heart failure or shock.
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Histotoxic hypoxia
Failure of cells to use O2 because they have been poisoned. Caused by cyanide and other metabolic poisons.
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Total arterial O2 content components
Oxygen dissolved in plasma and oxygen bound to Hb
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Alveolar-blood gas exchange
Oxygen diffuses across alveolar epithelial cells and capillary endothelial cells to enter the plasma.
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Destruction of alveoli means less surface area for gas exchange
Emphysema
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Thickened alveolar membrane slows gas exchange. Loss of ling compliance may decrease alveolar ventilation
Fibrotic lung diseas
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Fluid in interstitial space increases diffusion distance. Arteriol pCO2 may be normal due to higher CO2 solubility in water
Pulmonary edema
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Increased airway resistance decreases alveolar ventilation
Asthma
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At equilibrium CO2 is ____ more soluble than O2
20 x
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Oxygen transport in the circulation and oxygen consumption by the tissues follows…
The principles of mass flow and mass balance, so they move down a concentration gradient
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Hemoglobin
Consists of four subunits, 2 alpha and 2 beta chains each centered around Fe2+
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Hb+O2–>HbO2
Oxyhemoglobin
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Hb-O2 binding is
Reversible and cooperative
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What is blood doping
Artificially improving ability to deliver more oxygen to muscles
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How much O2 is bound to Hb in red blood cells
More than 98%
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How much O2 is dissolved in plasma
2%
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What membrane layers does O2 diffuse through to attach to an RBC
1) alveolar
2) basement membrane
3)capillary endothelium
4) cell membrane of RBC
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Why do we need Hb for oxygen transport
A persons O2 consumption at rest is about 250 mL O2/min adn the cardiac output is 5Lblood/min. At normal Hb levels red bloods cells carry 197 mLO2/L blood while 3 mLO2/Lblood will be dissolved in the plasma
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How does hemoglobin influence O2 transport
4X more O2 is available than is needed by cells at rest
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How does plasma pO2 influence O2 transport
Plasma pO2 is the primary factor determining what percentage of the available hemoglobin binding sites are occupied by O2, known as the percent saturation of hemoglobin.
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Three determinants of arterial pO2
Gas composition of inspired air, alveolar ventilation rate, efficiency of has exchange between alveoli and blood
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Altitude sickness
Leads to decrease in the pO2 at all points along the transport cascade. Decreased alveolar and arterial oxygen tensions trigger physiological responses form across multiple organ systems.
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Symptoms of altitude sickness
Increases HR, increases respiratory rate, increased frequency of urination, dyspnea, poor sleep, transient lightheadedness upon assuming upright position
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A right shift of the O2-Hb curve
Indicates a decrease hemoglobin affinity for oxygen, thus oxygen actively unloads.
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A left shift on the O2-Hb curve
Indicates an increase hemoglobin affinity for oxygen, this reluctance to release O2
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What does CO2 react with to form carbonic acid
Water. And increased CO2 in plasma results in lower blood pH. Hb releases oxygen.
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Decreased CO2 in plasma
Provokes an increased blood pH and hemoglobin picks up and retains oxygen
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Increased temperature does what to the O2-Hb curve
Decreases the affinity of Hb for oxygen so moves it right
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Decreases 2,3-BPG does what it the O2-Hb curve
Increases the affinity of Hb for oxygen so shifts the curve left.
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Fetal hemoglobin has a protein structural change that causes what
Enhances oxygen binding and causes the curve to shift left
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What does Hb have a greater binding affinity for than O2
Carbon monoxide by 200-300 times
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Carbon dioxide transport mechanisms
Dissolved in plasma (7%), bound to Hb (23%), converted to bicarbonate ion (70%)
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What affect on blood acidity does breathing out CO2 have
Decreases it
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What is ventilation based on
Chemoreceptor and mechanoreceptor reflexes modulated by the brain stem neurons.
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What neurons in the medulla control inspiratory and expiratory muscles
The NTS, DRG and VRG
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Pons
PRG receives sensory information from the DRG which influences the initiation and termination of respiration. It also coordinates a smooth respiratory rhythm
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What is the primary stimulus in regulating ventilation
CO2, O2 and pH play a lesser role
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Peripheral chemoreceptors
Located outside of CNS, primarily in carotid and aortic bodies, always exposed to arterial blood. Sense changes in CO2 and O2 and pH. But to respond to them pO2 < 60mmhg which happens only In unusual physiological conditions.
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What do carotid and aortic oxygen sensors do when snes pO2 decrease (below 60mmHg)
They release neurotransmitters
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How do pH changes in plasma influence CNS chemoreceptors
Not directly. CO2 has to enter CSF b/c it can cross BBB quickly and H+ ions cross very slowly
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Irritant receptors
The airway epithelium is lined with irritant receptors that are stimulated by irritants that enter the respiratory airways. Bronchoconstriction and coughing are the protective reflex
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Stretch receptors
Increase in tidal volume activates these in the lung to signal the brain stem to terminate inspiration. Also called the Hering-Breuer inflation reflex
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What monitors blood gases and pH
Central and peripheral chemoreceptors
